Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326
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Jing Ke1,2, Yi-long Yao3, Jian Zheng3, Ping Wang1,2, Yun-hui Liu3, Jun Ma1,2, Zhen Li3, Xiao-bai Liu3, Zhi-qing Li1,2, Zhen-hua Wang4, Yi-xue Xue1,2
1Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, China
2Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, China
3Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, China
4Department of Physiology, College of Basic Medicine, China Medical University, Shenyang 110122, China
Yi-xue Xue, e-mail: firstname.lastname@example.org
Keywords: lncRNA, HOTAIR, miR-326, glioma, FGF1
Received: February 07, 2015 Accepted: June 17, 2015 Published: June 27, 2015
Glioma is the most common and aggressive primary adult brain tumor. Long non-coding RNAs (lncRNAs) have important roles in a variety of biological properties of cancers. Here, we elucidated the function and the possible molecular mechanisms of lncRNA HOTAIR in human glioma U87 and U251 cell lines. Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.
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